scispace - formally typeset
J

Janet D. Sparks

Researcher at University of Rochester Medical Center

Publications -  90
Citations -  9589

Janet D. Sparks is an academic researcher from University of Rochester Medical Center. The author has contributed to research in topics: Apolipoprotein B & Insulin. The author has an hindex of 38, co-authored 89 publications receiving 8951 citations. Previous affiliations of Janet D. Sparks include Indiana University & Wistar Institute.

Papers
More filters
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Insulin modulation of hepatic synthesis and secretion of apolipoprotein B by rat hepatocytes

Janet D. Sparks, +1 more
- 25 May 1990 - 
TL;DR: Results demonstrate that an intracellular pool of apoB, primarily apoBL, exists that is largely unaffected by insulin, and insulin action in primary hepatocyte cultures reduces the secretion of freshly synthesized apolipoprotein B and favors secretion of preformed apo B enriched in apo BL.
Journal ArticleDOI

Insulin regulation of triacylglycerol-rich lipoprotein synthesis and secretion

Janet D. Sparks, +1 more
- 17 Nov 1994 - 
TL;DR: This review has considered a number of observations obtained from studies of insulin in perfused liver, hepatocytes, transformed liver cells and in vivo and each of the experimental systems offers advantages and suggests that insulin is stimulatory to the production of hepatic TRL in vivo.
Journal ArticleDOI

The triple threat to nascent apolipoprotein B. Evidence for multiple, distinct degradative pathways.

Edward A. Fisher, +7 more
- 27 Jul 2001 - 
TL;DR: F nascent apoB is subject to ER-associated degradation, re-uptake, and a third distinct degradative pathway that appears to target lipoproteins after considerable assembly and involves a post-ER compartment and PI3K signaling.
Journal ArticleDOI

Selective Hepatic Insulin Resistance, VLDL Overproduction, and Hypertriglyceridemia

Janet D. Sparks, +2 more
- 01 Sep 2012 - 
TL;DR: The role of insulin–related signaling pathways that determine hepatic VLDL production are summarized and a number of pathways are altered that further augment V LDL hypersecretion, including hepatic inflammatory pathways.